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Volume 10, Number 3—March 2004

West Nile Poliomyelitis

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To the Editor: In the July 2003 article, “Acute Flaccid Paralysis and West Nile Virus Infection” (1), Sejvar et al. reported seven patients with acute onset of asymmetric weakness and areflexia but no sensory abnormalities. The authors also referenced three previously reported cases of West Nile virus (WNV)–associated flaccid paralysis and argued that all of these symptoms could be explained by anterior-horn cell loss. The two cases of spinal cord pathologic findings published to date demonstrated focal loss of anterior-horn neurons (2,3). We report a case of West Nile poliomyelitis with preserved deep-tendon reflexes, diminished sensory nerve action potentials, and pathologic findings which do not localize to the anterior horn.

An 83-year-old woman sought treatment at the hospital on September 12, 2002, with 3 days of fever, acute confusion, nausea, vomiting, and profound weakness. Computed tomography (CT) of the head was unremarkable. Her examination was notable for dysarthria, tremors, and global weakness with rightsided predominance. Cerebrospinal fluid contained 75 leukocytes/mm3 (84% neutrophils), glucose 88 mg/dL, and protein 97 mg/dL. On the second hospital day, respiratory failure developed, requiring mechanical ventilation. Electrodiagnostics performed on hospital day 7 demonstrated reduced motor and sensory amplitudes on right median and ulnar nerves, reduced motor amplitudes, and mildly reduced conduction velocities in the right peroneal nerve and right posterior tibial nerves. These findings suggested a predominantly axonal polyneuropathy involving both sensory and motor nerves. No myopathic process was demonstrated. Serum antibodies for WNV (immunoglobulin [Ig] M capture enzyme-linked immunosorbent assay [ELISA] 73.8; IgG capture ELISA 0.738) and cerebrospinal fluid antibody titer (IgM capture ELISA 200.5) were both positive. Weakness, respiratory failure, and preserved deep-tendon reflexes persisted.

On hospital day 15, the patient died after withdrawal of support. Sections from the postmortem medulla and spinal cord were positive for WNV RNA by reverse transcription–polymerase chain reaction testing at the state laboratory. The brain demonstrated characteristic microglial nodules and perivascular lymphocytic infiltrates (4). Spinal cord sections showed leptomeningeal and parenchymal chronic inflammatory infiltrates, often perivascular in location. Patchy cellular infiltration was found throughout the spinal cord, without a predilection for the anterior-horn. Spinal nerve roots demonstrated focal lymphocytic inflammation within the endoneurial compartment. No evidence of a demyelinating process was found.

Our data contradict the thesis proposed by Sejvar et al. that West Nile poliomyelitis is restricted to the anterior-horn (1). The electrodiagnostics showing axonal polyneuropathy and the spinal cord pathologic findings, which did not demonstrate focal loss of anterior-horn neurons, suggest a broader spectrum of the clinical-pathological syndrome of West Nile poliomyelitis than previously described (2,3). Our findings conform to the hypothesis outlined by Jeha et al., which favors a more widespread myelitis (5). We also confirm the findings of preserved deep-tendon reflexes in West Nile poliomyelitis first reported by Glass et al. (6).


Robert P. Holman*Comments to Author , Nicole M. Monserrate*, Eric W. Czander*, and Elisabeth J. Rushing†
Author affiliations: *Virginia Hospital Center, Arlington, Virginia, USA; †Armed Forces Institute of Pathology, Walter Reed Army Medical Center, Washington, DC, USA



  1. Sejvar  JJ, Leis  AA, Stokic  DS, Van Gerpen  JA, Marfin  AA, Webb  R, Acute flaccid paralysis and West Nile virus infection. Emerg Infect Dis. 2003;9:78893.PubMedGoogle Scholar
  2. Kelley  TW, Prayson  RA, Isada  CM. Spinal cord disease in West Nile virus infection [letter]. N Engl J Med. 2003;348:5645. DOIPubMedGoogle Scholar
  3. Kelley  TW, Prayson  RA, Ruiz  AI, Isada  CM, Gordon  SM. The neuropathology of West Nile virus meningoencephalitis: a report of two cases and review of literature. Am J Clin Pathol. 2003;119:74953. DOIPubMedGoogle Scholar
  4. Sampson  BA, Ambrosi  C, Charlot  A, Reiber  K, Veress  JF, Armbrustmacher  V. The pathology of human West Nile virus infection. Hum Pathol. 2000;31:52731. DOIPubMedGoogle Scholar
  5. Jeha  LE, Sila  CA, Lederman  RJ, Prayson  RA, Isada  CM, Gordon  SM. West Nile virus infection: a new acute paralytic illness. Neurology. 2003;61:559.PubMedGoogle Scholar
  6. Glass  JD, Samuels  O, Rich  MM. Poliomyelitis due to West Nile virus [letter]. N Engl J Med. 2002;347:12801. DOIPubMedGoogle Scholar


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DOI: 10.3201/eid1003.030593

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In Reply: The letter by Holman, et al. (1), in this edition of Emerging Infectious Diseases continues to broaden the scope of illness attributable to West Nile virus (WNV) infection. However, we would like to take the opportunity to clarify the conclusions drawn from our article, “AFP and West Nile virus infection” (2). In this article, we reported on seven patients, all of whom had asymmetric weakness without sensory loss, which evolved acutely over the course of several hours. Electrodiagnostic studies of all patients displayed markedly reduced compound motor axon potentials with preserved sensory nerve action potentials; the results were interpreted as consistent with a process primarily localized to the motor axons or, far more likely, given the clinical scenario and pathologic data from WNV-infected animals, the anterior horn cells of the spinal cord. These findings were later substantiated by Li et al. (3). Subsequently, Jeha et al. expanded the scope of illness producing WNV-associated flaccid paralysis by describing several patients with predominant myeloradiculitis (4).

The patient presented by Holman clearly seems to have a condition that, as shown by electrodiagnostics and pathology, localizes to other areas, in addition to spinal anterior horn cells. However, rather than suggesting that a single case report “contradicts” the anterior horn cell hypothesis, we suggest that WNV-associated flaccid paralysis be viewed as having a spectrum of causes, one of which certainly is poliomyelitis like illness.

The neuropathologic findings in poliomyelitis (due to poliovirus, WNV, or other viruses) are not restricted focally to the anterior horn cells (5). Demonstrating pathologic changes as well as focal anterior horn cell loss in the patient referenced by Holman is in keeping with neuropathologic findings in poliomyelitis. Additionally, the presence of a diffuse axonal polyneuropathy cannot be concluded from Holman’s data. Reduced compound motor axon potentials and slowing of conduction velocity could certainly be seen in pathologic conditions affecting anterior horn cells or spinal nerve roots. In addition, reduced sensory nerve action potentials in the median and ulnar nerves alone, without documentation of neuropathy in additional nerves, cannot be used as evidence of a diffuse axonal polyneuropathy, since both of these nerves are commonly prone to entrapment neuropathies. Finally, the context in which the preservation of this patient’s reflexes is observed remains unclear. Preserved “normal” deep-tendon reflexes, in the setting of disease that interrupts the reflex arc at any point, are incongruous with established physiologic and clinical concepts.

The seven patients observed by our group clearly had a distinct clinical syndrome with similar clinical findings and electrodiagnostic results. However, as demonstrated by prior reports (3,57), multiple mechanisms may lead to WNV-associated flaccid paralysis. In fact, we acknowledge a spectrum of cord, root, and nerve involvement with WVN flaccid paralysis.

James J. Sejvar, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop A39, 1600 Clifton Road, Atlanta, GA 30333, USA; fax: 404-639-3838
Author affiliations: *Centers for Disease Control and Prevention, Atlanta, Georgia, USA; †Methodist Rehabilitation Center, Jackson, Mississippi, USA; ‡Ochsner Clinic, New Orleans, Louisiana, USA; §Centers for Disease Control and Prevention, Fort Collins, Colorado, USA


  1. Holman  RP, Monserrate  NM, Czander  EW, Rushing  EJ. West Nile poliomyelitis. Emerg Infect Dis. 2004;10:5478. DOIPubMedGoogle Scholar
  2. Sejvar  J, Stokic  D, Van Gerpen  J, Marfin  A, Webb  R, AFP and West Nile virus infection. Emerg Infect Dis. 2003;9:78893.PubMedGoogle Scholar
  3. Li  J, Loeb  J, Shy  M, Shah  A, Tselis  A, Kupski  W, Asymmetric flaccid paralysis: a neuromuscular presentation of West Nile virus infection. Ann Neurol. 2003;53:70310. DOIPubMedGoogle Scholar
  4. Jeha  L, Sila  C, Lederman  R, Prayson  R, Isada  C, Gordon  S. West Nile virus infection: a new acute paralytic illness. Neurology. 2003;61:559.PubMedGoogle Scholar
  5. Paul  J. A history of poliomyelitis. New Haven (CT): Yale University Press; 1971. p. 1–9.
  6. Ohry  A, Karpin  H, Yoeli  D, Lazari  A, Lerman  Y. West Nile virus myelitis. Spinal Cord. 2001;39:6623. DOIPubMedGoogle Scholar
  7. Gadoth  N, Weitzman  S, Lehmann  E. Acute anterior myelitis complicating West Nile fever. Arch Neurol. 1979;36:1723. DOIPubMedGoogle Scholar

Table of Contents – Volume 10, Number 3—March 2004

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Please use the form below to submit correspondence to the authors or contact them at the following address:

Robert P. Holman, 1715 N. George Mason Dr., Suite 108, Arlington, VA 22205, USA; fax: 703-558-6657

James J. Sejvar, Division of Viral and Rickettsial Diseases, National Center for Infectious Diseases, Centers for Disease Control and Prevention, Mailstop A39, 1600 Clifton Road, Atlanta, GA 30333, USA; fax: 404-639-3838

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